Abstract
Neuroinflammation, which is involved in various inflammatory cascades in nervous tissues, can result in persistent and chronic apoptotic neuronal cell death and programmed cell death, triggering various degenerative disorders of the central nervous system (CNS). The neuroprotective effects of natural compounds against neuroinflammation are mainly mediated by their antioxidant, anti-inflammatory, and antiapoptotic properties that specifically promote or inhibit various molecular signal transduction pathways. However, natural compounds have several limitations, such as their pharmacokinetic properties and stability, which hinder their clinical development and use as medicines. This review discusses the molecular mechanisms of neuroinflammation and degenerative diseases of CNS. In addition, it emphasizes potential natural compounds and their promising nanocarriers for overcoming their limitations in the treatment of neuroinflammation. Moreover, recent promising CNS inflammation-targeted nanocarrier systems implementing lesion site-specific active targeting strategies for CNS inflammation are also discussed.
Highlights
Various central nervous system (CNS) disorders, CNS degenerative diseases including Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), multiple sclerosis (MS), and amyotrophic lateral sclerosis (ALS), have become a bigger burden to individuals, families, and society, the molecular mechanisms and microenvironments of these disorders have not been fully understood
A recent study reported that gallic acid inhibited the production of Reactive oxygen species (ROS), disruption of mitochondrial membrane potential, and expression of Bax and caspase-3, and it promoted the expression of Bcl-2 and brain-derived neurotrophic factor (BDNF) and upregulation of the Nuclear factor erythroid 2-related factor 2 (Nrf-2) and cyclic adenosine monophosphate response element-binding protein (CREB) pathways, thereby protecting neuronal cells from neurodegeneration in a PD model [102]
Neuroinflammation, which is involved in various inflammatory cascades, occurs by microglia/astrocytes activation, oxidative stresses, and mitochondrial dysfunction in the nervous tissue, and it can result in persistent and chronic apoptotic neuronal cell death and programmed cell death, thereby triggering various CNS degenerative disorders
Summary
Various central nervous system (CNS) disorders, CNS degenerative diseases including Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), multiple sclerosis (MS), and amyotrophic lateral sclerosis (ALS), have become a bigger burden to individuals, families, and society, the molecular mechanisms and microenvironments of these disorders have not been fully understood. Their pharmacological effects on neuroinflammation are often impeded because of their instability, poor solubility, and/or poor blood–brain barrier (BBB) permeability, resulting in lower bioavailability (BA), lower distribution in target tissue (brain), and higher systemic toxicities [15,16] To overcome these limitations and improve their pharmacokinetic properties and stability, the role of various nanocarriers (e.g., polymeric nanoparticles (NPs), micelles, lipid NPs, liposomes, inorganic NPs, exosomes, and carbon-based NPs) have been emphasized recently, in clinical trials. We discuss recent advances in therapeutic strategies for targeting CNS inflammation as well as the limitations in clinical trials
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